Professor H Terence Cook

Terry Cook FMedSci is Professor of Renal Pathology and Deputy Director of the Centre for Complement and Inflammation Research at Imperial College. He is also Consultant Renal Pathologist in the Imperial Academic Health Science Centre. He is Past-President of the Renal Pathology Society.

Research Interests

My major interest is in elucidating mechanisms of injury in glomerulonephritis. We have used a number of models of induced and autoimmune glomerulonephritis to explore the role of macrophages, antibodies, Fc receptors, complement and other mediators. We have also studied genetic influences on susceptibility to glomerulonephritis and to autoimmunity. We are currently investigating the genes that control macrophage activation and the contribution of these to crescentic glomerulonephritis.

Clinical Research

I have a major interest in how histological features in human renal biopsies can be used to predict outcome and response to treatment. I have organised international collaborative studies to develop consensus classifications of lupus glomerulonephritis, IgA nephropathy and diabetic nephropathy. We are currently studying the predictive value of transcript analysis in biopsies of transplant kidneys.

SELECTED KEY PUBLICATIONS

Baruah P, Simpson E, Dumitriu IE, Derbyshire K, Coe D, Addey C, Dyson J, Chai JG, Cook T, Scott D, Botto M: Mice lacking C1q or C3 show accelerated rejection of minor H disparate skin grafts and resistance to induction of tolerance. Eur J Immunol. 2010, 40(6):1758-1767.

Cattran DC, Coppo R, Cook HT, Feehally J, Roberts IS, Troyanov S, Alpers CE, Amore A, Barratt J, Berthoux F, Bonsib S, Bruijn JA, D'Agati V, D'Amico G, Emancipator S, Emma F, Ferrario F, Fervenza FC, Florquin S, Fogo A, Geddes CC, Groene HJ, Haas M, Herzenberg AM, Hill PA, Hogg RJ, Hsu SI, Jennette JC, Joh K, Julian BA, Kawamura T, Lai FM, Leung CB, Li LS, Li PK, Liu ZH, Mackinnon B, Mezzano S, Schena FP, Tomino Y, Walker PD, Wang H, Weening JJ, Yoshikawa N, and Zhang H: The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification. Kidney Int 2009, 76: 534-545

Roberts IS, Cook HT, Troyanov S, Alpers CE, Amore A, Barratt J, Berthoux F, Bonsib S, Bruijn JA, Cattran DC, Coppo R, D'Agati V, D'Amico G, Emancipator S, Emma F, Feehally J, Ferrario F, Fervenza FC, Florquin S, Fogo A, Geddes CC, Groene HJ, Haas M, Herzenberg AM, Hill PA, Hogg RJ, Hsu SI, Jennette JC, Joh K, Julian BA, Kawamura T, Lai FM, Li LS, Li PK, Liu ZH, Mackinnon B, Mezzano S, Schena FP, Tomino Y, Walker PD, Wang H, Weening JJ, Yoshikawa N, and Zhang H: The Oxford classification of IgA nephropathy: pathology definitions, correlations, and reproducibility. Kidney Int 2009, 76: 546-556

Behmoaras J, Bhangal G, Smith J, McDonald K, Mutch B, Lai PC, Domin J, Game L, Salama A, Foxwell BM, Pusey CD, Cook HT, Aitman TJ: Jund is a determinant of macrophage activation and is associated with glomerulonephritis susceptibility. Nat Genet. 2008, 40(5):553-9.

Rose KL, Paixao-Cavalcante D, Fish J, Manderson AP, Malik TH, Bygrave AE, Lin T, Sacks SH, Walport MJ, Cook HT, Botto M, Pickering MC: Factor I is required for the development of membranoproliferative glomerulonephritis in factor H-deficient mice. J Clin Invest. 2008, 118(2):608-18.

Fanciulli M, Norsworthy PJ, Petretto E, Dong R, Harper L, Kamesh L, Heward JM, Gough SC, de Smith A, Blakemore AI, Froguel P, Owen CJ, Pearce SH, Teixeira L, Guillevin L, Graham DS, Pusey CD, Cook HT, Vyse TJ, and Aitman TJ: FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity. Nat Genet 2007, 39: 721-723

Smith J, Lai PC, Behmoaras J, Roufosse C, Bhangal G, McDaid JP, Aitman T, Tam FW, Pusey CD, and Cook HT: Genes expressed by both mesangial cells and bone marrow-derived cells underlie genetic susceptibility to crescentic glomerulonephritis in the rat. J Am Soc Nephrol 2007, 18: 1816-1823

Aitman TJ, Dong R, Vyse TJ, Norsworthy PJ, Johnson MD, Smith J, Mangion J, Roberton-Lowe C, Marshall AJ, Petretto E, Hodges MD, Bhangal G, Patel SG, Sheehan-Rooney K, Duda M, Cook PR, Evans DJ, Domin J, Flint J, Boyle JJ, PuseyCD, Cook HT: Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats and humans. Nature. 2006 ;439:851-855

Pickering, M.C., Cook, H.T., Warren, J., Bygrave, A.E., Moss, J., Walport, M.J. and Botto, M., Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H. Nature Genet. 4, (2002),:424-428